Nasal symbiont Staphylococcus epidermidis restricts influenza virus replication via the creation of a polyamine-deficient cellular environment

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Abstract Background Studies on the immune-regulatory roles played by the commensal microbes residing in the nasal mucosa consider the contribution of mucosal immune responses. Here, we sought to identify the nasal microbiome, Staphylococcus epidermidis-regulated antiviral immune responses and the alteration of polyamine metabolites in nasal epithelium. Results We found that polyamines were required for the life cycle of influenza A virus (IAV) and depletion of polyamines disturbed IAV replication in normal human nasal epithelial (NHNE) cells. Inoculation of S. epidermidis also suppressed IAV infection and the concentration of polyamines including putrescine, spermidine, and spermine was completely attenuated in S. epidermidis-inoculated NHNE cells. Interestingly, the activity of enzymes related to polyamine production was reduced and the cellular export of polyamines was activated in NHNE cells depending on S. epidermidis inoculation. Conclusion Our findings demonstrate that human nasal commensal S. epidermidis contributes to shape a polyamine-deficient cellular environment and restricts IAV replication in the nasal epithelium.

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